Coinfection is the simultaneous infection of a host by multiple pathogen species and is commonplace in vertebrate hosts. As pathogen species can (in)directly interact within the host, coinfections are considered to be of particular importance in the ecology of wildlife diseases. In general, pathogens do not exert their effects in isolation; they act in conjunction with other parasites infecting the host. The subject of coinfection is increasingly recognized as a complex process that breaks down the one-pathogen/one-disease paradigm, altering pathologic and immunologic effects in the host, the severity and duration of disease, and ultimately transmission in ways that are different, and often greater, than would be expected from single infections. In this project, I test the hypothesis that directly-transmitted Mycoplasma (MG) will transmit more efficiently when interacting with common songbird copathogens (Plasmodium relictum (PR), a mosquito-transmitted protozoan, and Borrelia burgdorferi s.s. (BB), a tick-borne bacterium), with coinfections exacerbating MG disease and transmission. Furthermore, I anticipate characterizing aspects of MG adaptation to the coinfected ‘host environment’.
The current COVID-19-crisis is providing ample evidence for pathogen evolution at rapid rates, fitness advantages allowing.
The objectives of this project - of which hypotheses have been tested within wild bird species - therefore are of high socio-economic value: understanding underlying processes of co-pathogen interactions on transmission dynamics is key to predict fitness landscapes favouring the one strain over the other, and therefore the population dynamics of both pathogen and host.
